Abstracts
 

Hello All,

I have not said a lot since joining this site as I tend to speak when something needs to be said only. I have edited much of this to facilitate easier understanding but one just cannot avoid some jargon.

I chose to use only one example of corruption of the scientific method - trust me, there are many others.

IN NO WAY DO I CLAIM RESEARCHERS ARE ALL CROOKED. IT IS A POLITICAL THING. (Please excuse the shouting).

Regarding the use of ABSTRACTS
Just a few notes to hopefully help some of you navigate the mire of misdirected scientific research and how the public can be mislead into making a judgement call when they rely on accepting the recommendations of doctors if they also choose to use these due to time constraints – ABSTRACTS THAT IS.
I have seen it noted that some people have used hundreds of ABSRACTS to form their ideas. This is at the very least worrisome.
This document is written from the perspective of a trained scientist (me) so I am writing within my own experience and its purpose is to clarify.

The true purpose of an abstract is to present an accurate precis of the work undertaken that is a quick study to tweak the interest of readers – whetting their appetite if you will. Unfortunately, this process has become corrupted with carefully chosen wording to make it (the Abstract) say what the orchestrators of the study wanted…..a slight of word if you will and with time short – it is taken as a full register of the theme of the work.

It is rare for a study to be designed with realistic analysis in mind - they try to fit the analysis in later. This too is questionable.

The only way to resolve this is to read the WHOLE ARTICLE which requires an understanding of statistics (not simply P<0.1 statements). These are pretty much meaningless by themselves. It also requires knowledge of the scientific method let alone the mechanisms physiology and anatomy and in our case biochemistry being studied.

To use an example that does not require deep understanding, the way in which Cognitive Behavioural Therapy (CBT)has leapt to prominence as being considered to be supported by Level I evidence (the highest level) raises issues when a lot of posted research is read IN DETAIL. The truth is (CBT) is done in groups because it is cheap (well documented by the British Health System) and the results for pain studies are largely based on Lower Back Pain studies – it is very difficult to find legitimate work relating to CRPS / RSD. What does happen is the work is interpolated or extrapolated to include ALL pain.

Additionally, the statistics are highly questionable. It is NOT ACCEPTABLE practice to allow crossover from a control group to a study group and many of the studies of CBT do just this. Further, they also allow the size of the study groups to be small – another statistical faux pas. They also seem content in many studies just to run with a few %’s and call them valid statistics….oops!
When meta-analyses are done to try to validate much of this work it is discounted in quite large quantities. Thus, only a small amount of the work out there can be regarded as legitimate for CRPS / RSD.

Now, where does that leave US?
Those of us who read only the ABSTRACT are left in the lurch with misinformation and problemlatic dogma in many cases. The remainder of the article often needs to be purchased from reputable sources such as Elsevier. This is understandable as these articles are in depth medical studies from highly reputable institutions.
As a scientist and yes I do have severe CRPS, it worries me that some people address numerous topics with such authority based on ABSTRACTS when they are using, at best, aged, misdirected and fragmented opinion. This opinion is frequently presented in forums whereby the uninitiated and perhaps not so-well informed trust those words written by those promulgating knowledge that is at best a sketchy twisting of the scientific method.
CHOOSE CAREFULLY AND WISELY my friends.....please!
I worry for our future.

I wish you all the very best success in finding something and someone to help ease your pain.

Auberon

Auberon,

A very thought provoking post. Thank you for putting that perspective out there for us to digest.
Even though I do have 30 years of working in the medical field and thus slightly higher than average understanding of medical jargon, I find the confusion these abstracts can cause incredibly frustrating.
I plod through so much of it and find that much is quite outdated and often a very subjective opinion of a medico with a mission.
Many of us here are more than happy to do our own research but many would rather depend on what others post and this is when the confusion can take hold. So many conflicting opinions and heated discussion which could well be helped by reading the whole article on the topic at hand.
Regards
Tayla

Hi Auberon,

I am one of those who use abstracts in my research, and I do it for a couple of reasons: Articles are filled with statistical information that is of no ues to me, I passed my statistics classes in the early 1970s and as soon as I walked out of finals I forgot 90% of everything I learned; I can't afford to pay the $20.00 to $60.00 to even more that many articles cost, and articles are so filled with words and phrases I've never seen before and it would take hours to learn them.

Abstracts provide the basic information I need: The goal of the research; the methods or instrument, and the conclusions.

When I first began researching RSD I had no idea what I was doing, and I saved a lot of useless stuff. As I became more discerning, I learned to ignore abstracts that didn't discuss some sort of research (and that's about 90% of the literature on this disease: Just someone's opinion on what happens).

When I moved on to learning about the immune system, oxygen free radicals, polymorphonuclear leukocytes, phagocytes, etc, I found fewer opinions and more research. Over time I could see when several research articles reached the same conclusions and concluded that widespread agreement is a good predictor of reliability.

I have also seen many examples of research designed to lead to the conclusion the researcher wanted to reach, and became a better judge. I have even learned enough about RSD, IRI, nerves and circulation to identify fatal flaws in research design, and even to tell when a "researcher" is just plain lying.

As you probably noted in my post to Mike, I noted that the stuff he presented had nothing to do with the topic: whether there are psychological factors predisposing someone to RSD. I pointed out that if the material didn't discuss RSD AND psychology, it doesn't apply.

I would prefer to find lots of research abstracts about the etiology of RSD, but neither they, or full articles exist. I am faced with the choice of giving up because I can't find what I want, or pressing on to learn what I can.

My conclusion that RSD is an ischemia-reperfusion injury (IRI) is based upon the fact that I know that nerves and nervous systems don't do what RSD "experts" tell us they do; and that impaired microcirculation can cause the signs and symptoms the "experts" falsely claim that our nerves cause. And the signs the "experts" pretend don't exist.

When I came across IRI I was forced to learn about the immune system and oxygen free radicals, and when I finally understood that disorder I realized that it starts the same way RSD starts; progresses the same way RSD progresses, and; ends with plugged microvascular systems, which is the only explanation for our signs and symptoms.

I know I will have a more dfficult time persuading people that RSD is IRI than I would have if I wore a lab coat and had a rectal thermometer in my pocket, but I do what I can, and all I can do is keep posting what I've learned until people begin to understand that I do know what I'm talking about.

When that happens, they will understand that hyperbaric oxygen (HBO) has a mechanism of action that does affect RSD and can lead to a better life. When that happens, I will have accomplished something worthwhile. I don't think any of this could happen if I had not relied upon abstracts...Vic

As a rule, I try to get my hands on the full texts of as many articles as possible, often through the kind assistance of a friend of mine who can just access his university's data base. Then again, sometimes I just pull out my credit card and buy them.

And to refer for a moment to the thread Vicc cited, the only article for which I did not provide access to a full text copy was one directly (as in absolutely) related to the topic at hand, RSD and stress: "Stressful life events and psychological dysfunction in Complex Regional Pain Syndrome type I.," Geertzen JH, de Bruijn-Kofman AT, de Bruijn HP, van de Wiel HB, Dijkstra PU, Clin J. Pain, 1998 Jun; 14(2): 143-7. Nevertheless, I regretted having only the abstract available.

Mike

Mike,

I don't have friends with access to articles, but as I said, they are less useful to me than abstracts.

And I did not complain about your lack of articles; in fact, I believe you post too many: Articles so filled with medspeak that no one here can possibly understand them. If you can't understand the words, you can't understand the sentences, the paragraphs or the article.

In my mind, this is a variation of "If you can't dazzle them with brilliance, baffle them with ********"

What I said in my reply was that nothing you posted (including the Geertzen abstract), had anything to do with a psychological predisposition to RSD. I'd be interested in seeing a reply that discusses this...Vic

My conclusion that RSD is an ischemia-reperfusion injury (IRI) is based upon the fact that I know that nerves and nervous systems don't do what RSD "experts" tell us they do; and that impaired microcirculation can cause the signs and symptoms the "experts" falsely claim that our nerves cause. And the signs the "experts" pretend don't exist.


Vicc,
Can you please, please explain how you "know that nerves and nervous systems don't do what RSD "experts' tell us they do, and that impaired microcirculation can cause the signs and symptoms the "experts" falsely claim that our nerves cause. And the signs the "experts' pretend don't exist" ?

Are we to believe that these people who spend years and years researching this disease are NOT experts but you are?
Please explain so that we can choose to not believe every single article about RSD that tells us that RSD is in fact a neurological disease.
Why would everyone one of these 'experts" whose opinions you clearly disagree with get it wrong?
We are not just talking USA here , but everywhere in the civilised world where research of RSD/CRPS takes place. There are a multitude of extremely intelligent people amongst them, why would they want to intentionally deceive us.
Sorry, it makes no sense to me but am happy to change my mind if you can provide a reason for me to do so.
Tayla

Tributes & Question
 

Hello,
Debate WITHOUT sour comment is just what we need to get our creative juices flowing. Not preaching one view over another. Should we not close the mouth & open the mind politely. For goodness sake, aren’t we trying to understand what has happened to our lives and we ALL need to pull together.
1. Numbers were designed to lie – that is the aim of statistics whether you use Euclidian or other base 22 systems.
For Michael: I agree and even though the Clinical Journal of Pain Articles can be difficult to grab they help. The small price for the few select articles I have purchased have been worth their weight in gold as they are right on the money.
I find your posts of great value.
My life is so down the tubes with this thing that I would delight in any genuine progress.
I am hugely concerned with improving my quality of life(QOL) – and should I find a valid approach I would be more than willing to share….the trouble is it doesn’t yet exist.
We may be looking in the wrong areas – and perhaps should be looking towards stem cells (our own) to lift QOL and account for demyelination & the unexplained things nerves can cause / do or whatever the hell causes this.
2. FOR ALL READERS:
My present problem is that body systems cannot be considered in isolation.
We are a WHOLE BEING – a system that interacts (I’m sorry this is put so simply).
For Tayla thanks for the comments….I have had significant issues with opinionated and ill-informed medical consultants. I think we ALL need to remember that a doctor is a paid consultant – not a GOD and this is the reason we need to be so well informed.
Vicc: I have ONE question and would like to address just ONE question at a time from what you have raised. First, an abstract that doesn’t discuss some method / process is an Extension Article written for people without the technical base to understand the article.
Abstracts are designed to get more research dollars – it is a process.
If I read your posts correctly, as I understand the terms, phrases etc I appear to be either full of ******** with some kindred spirits or I have a superfluous thermometer uncomfortably placed.
So to the question Vicc:
I read that Abstracts provide the basic information you need and should you see that any research of any kind has been done with your key words that it is OK and assumed correct. No further work required, even if that research has been corrupted through numbers and crossover from control groups has been allowed.
IS THIS CORRECT?
An abstract cannot contain sufficient information to judge this and there are enough free articles to help with whole article access. You do go to a lot of trouble to defend the shortcut method of just relying on abstracts when you have a barrel to push at people without the support of logic and science.
The numbers are easily made to lie so they can say what they want to get more $.
Just a note: Peer review in medicine doesn’t work. So that is not an out.

Tayla,

I challenge you to find any evidence of any disorder caused by nerve damage that can simulatneously affect skin; bone; muscle; nerves and the vascular system, one that can affect afferent and efferent nerves of the peripheral and sympathetic nervous systems, AND can simply wander where it will throughout the body.

If you can do that, drop a note to the National Institute for Neurological Disorders and Stroke, because in 2006, it repoted "The cause of CRPS is not known" [1].

Are we to believe that these people who spend years and years researching this disease are NOT experts but you are? Yup. These people who spent years "researching" RSD have not yet published a single article linking this disease to nerve damage. They claim it, but they can't prove it.

There are a multitude of extremely intelligent people amongst them, why would they want to intentionally deceive us. I have several ideas about why they would want to deceive us, but nothing to prove any of them. Why not ask they why they refuse to even mention the word cyanosis? Every time they publish a list of signs and symptoms of this disease and omit cyanosis, they are deceiving us.

These are just brief yet compelling arguments, others can be found in posts I've made in the past, while still others -- specifically why traumatic nerve damage cannot cause the pain associated with RSD -- will appear in the future.

If you want to argue that traumatic nerve damage causes all of the signs and symptoms of RSD, why not find some research that confirms this? Vic

Afterthought: Since it appears to be widely accepted that CRPS-I (the overwhelming majority of RSD cases) is NOT caused by nerve damage, why do you insist that it is?

Cyanosis
 

Vicc, greetings,
CYANOSIS is a medical descriptive term for the bluish appearance of poorly oxygenated (generally) peripheral tissues.
It gives no indication of cause. Determining cause is the clinicians’ job.
It just is bluish tissue.
It is not a disease state. I think too much credence is being given to an innocuous sign / symptom of an underlying diseased state.
Cyanosis has a cause – a multitude of causes in fact – it can be a cold limb, poor venal flow, poor capillary flow or poor performance of the heart due to arterial plaque just to name a few. It can be due to substance P and its effect on other tissues. I also believe some cyanosis can be presented by ADP affecting mitochondrial respiratory process...but this is a stretch. It can also be due to the NADH going awry in the Krebs cycle. ALL CAUSES.

The question is why have these things caused the cyanosis?

Every mammal can express it and the causes are always the same. It is one of the signs and symptoms of small stomach worm infestation in all mammals and occurs in the mucosal membranes. In fact when managing flock animals it is the first sign one looks for to indicate internal parasites. They are being bled to death by the worms. SIGN derives CAUSE derives TREATMENT derives (if caught soon enough) well animal with pink membranes.

So I am confused as to how this has become the spectre causing RSD / CRPS.
It is derived from the Greek language and in no way implies the presence of cyanide (HCN).
Clarification would be greatly appreciated Vicc.

Appreciate the time. Auberon

Auberon,

Had you not written: I have seen it noted that some people have used hundreds of ABSRACTS to form their ideas. This is at the very least worrisome. I would not have commented here at all.

Since I am (to my knowledge) the only person here to have written about extensive use of abstracts, and I only wrote those words days ago, I have to assume that was directed toward me and that others would read those words -- written by a scientist -- and assume I must be irrelevant. A reply was necessary.

Here is how I used abstracts to conclude that explanations for traumatic nerve damage as the cause of RSD are nonsense, and why abstracts convinced me that ischemia-reperfusion injury explains every sign and symptom of this disease.

I read, or skimmed, hundreds of abstracts about RSD that I found at PubMed and MedScape, and didn't find a single one that referred to research showing that nerve damage causes RSD. Had I found such an abstract, I might have paid money to read the full article.

Thousands of people who suffer from this disease die every year, yet I have not seen a single abstract describing necropsies that found nerve damage. The one abstract that did involve necropsies found minor nerve damage in a few of the samples, but NONE that could explain the signs and symptoms of this disease [1].

In my review of abstracts on the subjects of the immune response to trauma, oxygen free radicals (OFRs) and ischemia-reperfusion injury (IRI), I found many describing in VIVO and in VITRO research, and all of them substantially agreed with one another.

The cause and course of IRI is clearly understood and almost universally agreed upon, and I was able, with my lay-persons education, augmented by what I had learned by more than two years of my studies, to extrapolate how every sign and symptom of RSD (including symptom migration) is explained by IRI.

2. FOR ALL READERS:
My present problem is that body systems cannot be considered in isolation.

Auberon, my problem is that every neurological explanation of RSD is just that: Limited to one body system; the nervous system. And none of the conclusions I found were supported by objective research. The bottom line with all of them is: "Because I'm an expert and I say so".

Vicc: I have ONE question and would like to address just ONE question at a time from what you have raised. First, an abstract that doesn’t discuss some method / process is an Extension Article written for people without the technical base to understand the article.

I found many abstracts discussing RSD that didn't require much in the way of technical understanding, but unfortunately, none of them made a bit of sense.

In order to understand IRI, one must understand the immune response to trauma and specifically the role of polymorphonuclear leukocytes and OFRs in that response. It took me nearly two years to feel confident that I had learned enough about them, so some technical knowledge is necessary, but such knowledge is not beyond the lay-persons ability to understand.

If I read your posts correctly, as I understand the terms, phrases etc I appear to be either full of ******** with some kindred spirits or I have a superfluous thermometer uncomfortably placed.

I don't know whether you carry a rectal thermometer, but your claim to be a scientist does conjure the image of the lab coat (and ya gotta admit that was an eye-catching line: I stole it from Lewis Black). If you place yourself in league with "experts" who don't use science to explain RSD, I guess you are full of ******** too.

I am hugely concerned with improving my quality of life(QOL) – and should I find a valid approach I would be more than willing to share….the trouble is it doesn’t yet exist. Why not investigat IRI? Your education and training should allow you to reach some conclusions in far less time than I took; and if you disagree with me you will have scientific reasoning to support your view.

(Others would find such a discussion/debate incredibly uninteresting, but I would be overjoye to find someone who could discuss that topic).

For Michael: I agree and even though the Clinical Journal of Pain Articles can be difficult to grab they help. The small price for the few select articles I have purchased have been worth their weight in gold as they are right on the money.

First, Mike doesn't just post articles from that journal; almost any article that mentions Il-6 is fair game for him, and I daresay you would have a difficult time understanding all the medspeak found in them. The rest of us can't understand a bit of it, so these articles are virtually useless.

Second, at the risk of calling in a new plague of medspeak, why not share one of these priceless articles with us? Just try to limit yourself to research that addresses RSD specifically, and not chronic pain, which is vastly different...Vic

(added later): The program somehow made the font on my tag line much smaller than intended, and the edit option does not allow one to change font size. Sorry about that.


A [ ] with a number inside means I will email you a copy of the article cited. Just click the “rsd_hbot” link at the bottom of the page and type in the title of the post and the number(s) you want to receive.

Auberon,

I'm always busy working on posts that discuss aspects of IRI that explain RSD, but always welcome the opportunity to talk about cyanosis.

CYANOSIS is a medical descriptive term for the bluish appearance of poorly oxygenated (generally) peripheral tissues. Precisely! In my thread Facts you may not know about RSD, I described how ischemia can cause cyanosis. My next post on that thread will discuss how ischemia causes severe hypersenstivity to lower ambient temperature and lower skin temperature in RSD. The third post will show how ischemia can cause every other sign an symptom of chronic (stage II) RSD.

It [cyanosis] is not a disease state. I think too much credence is being given to an innocuous sign / symptom of an underlying diseased state.

I dispute your contention that cyanosis is an innocuous sign: It is visible evidence of death, and nearly every incident of dark cyanosis is treated as an emergency that must be treated to save the life or limb of the patient. It is ignored in only one disease: RSD.

You list multiple causes for cyanosis, and you're correct; but the cause of cyanosis can be discovered, if only by excluding every other possible cause. Unless you wish to argue that one of the causes you mentioned is responsible for cyanosis in RSD, then I claim that IRI wins by default.

You can, of course, argue that IRI is not the cause of cyanosis in RSD, but in order to do that you will need to learn something about IRI. I suspect that if you do, you will conclude, as I did, that IRI does cause cyanosis in RSD.

In the years that I have been arguing that RSD is IRI, I have been personally attacked by several people (apparently outraged that someone WITHOUT a rectal thermometer dares to argue with "experts" who are legally allowed to carry one). Many of these attacks come in the form of deliberately misquoting me or summarizing my views in dishonest ways.

I don't assume that just because you wrote So I am confused as to how this has become the spectre causing RSD / CRPS. that you are deliberately and dishonestly summarizing my views, but I have been very careful NOT to say that cyanosis causes RSD.

Cyanosis does not cause RSD. It is a sign of ischemia-reperfusion injury, and that is the cause of this disease...Vic

OK I have to step in...

Vicc.. you are asking us to prove to you that RSD is a neurological condition, and you cant prove that IRI is RSD or that IRI causes RSD... ??? you even said that you dont have written proof of this or stuff on the internet??? Confused again...

Amber

Vicc,

I hope these lines find you doing well. You and everyone else know I have a very open mind about RSD.

What do you think is the underlying cause of the ischemia? I believe the root of my problem is infection. In my life I have only heard of 2 things that spread, INFECTION and CANCER. Hugs, Roz

http://stroke.ahajournals.org/cgi/co...keaha;26/3/373

The mechanisms linking infection and cerebral ischemia are still largely undetermined. In endocarditis, emboli from infected heart valves can cause ischemic stroke,29 and in bacterial, including tuberculous, meningitis, cerebral vasculitis can lead to ischemic stroke30 ; after herpes zoster of the neck and face, a local necrotizing arteritis can occur and can cause cerebral ischemia.31 However, these conditions were not present in our patients. Inflammatory mechanisms that accompany infection can stimulate coagulation by several pathways. These include the expression of thromboplastin by monocytes and macrophages,32 increased serum levels of tumor necrosis factor- and other cytokines33 34 that may alter coagulant function of the endothelium, the inhibition of the protein C/protein S anticoagulant system,35 36 and increased levels of clotting factors such as fibrinogen.2 In patients with infection-associated cerebral infarction, Ameriso and coworkers14 detected increased fibrin generation, increased cardiolipin immunoreactivity, and hyperfibrinogenemia compared with stroke patients without infections. This indicates a link between ischemic stroke, infection, and a procoagulant state. Further investigations are required to clarify the mechanisms linking acute infection and cerebral ischemia.

Amber,

Of course you have to step in; I would not have expected otherwise.

I am not asking you to prove that RSD is caused by a traumatic nerve injury, I am asking the "experts" to prove what they claim. I am saying that if you insist that this is the result of a nerve injury, and insist that I must be wrong, you should provide some evidence supporting your view or contradicting mine. I am still waiting for someone to do that.

I can't prove that RSD is an IRI: I argue that it is, and offer a great deal of evidence that supports this view, but my goal is to persuade others to investigate IRI for themselves and reach their own conclusions...Vic

Thanks for being soo nice Vicc...
:rolleyes:

I will look into what you asked me and will get back to you!! I dont think we understood what you asked of us... and now that you have come out and said it Im sure there will be posts regarding this!

Amber

Dear Auberon,

It's nice that you have come out of the closet.;) But in my opinion I believe something has entered my CNS, probally co-infections. Like maybe Bartonella being one for instance. http://en.wikipedia.org/wiki/Bartonella

What is your opinion on infections possiably being the root?

I am not sensitive at all. So I would appreciate your wisdom in anyway. Aren't several types of infections very slow growing? Much Love, Roz

Vicc,

I think these will help us say its Neurological.... and RSD is nerve involved. How else do you explain it hitting the ears and eyes, ect...

RSD PUZZLE #24
Visual And Hearing Problems


RSD patients frequently develop blurring of vision, reading difficulty, problem with focusing, dizziness in the form of vertiginous attacks (either the body or the objects moving around). As well as hearing problems such as buzzing in the ear (tinnitus).

It is immaterial which part of the body has had the damage causing RSD. As the enclosed figure shows, the sympathetic nervous system is intermingled and connected through sympathetic ganglia which are on each side of the vertebrae from lower cervical spine region all the way down to the tail bone. This chain of sympathetic connections causes the spread of RSD to symptoms and signs both across the midline to the opposite side (from hand to hand or from foot to foot) and vertically up and down the spine. As a result, the patient may have RSD due to a knee injury or injury to the foot or hand and yet may develop stimulation and abnormal function of the sympathetic system causing constriction of the blood vessels to the brain. When the blood vessels are constricted in the distribution of vertebral arteries in the cervical spine and in the distribution of the blood vessels providing circulation for the hearing center and brainstem, the patient develops attacks of dizziness, trouble with focusing with the eyes (due to brainstem dysfunction which has the responsibility of coordinating the eye movements), and buzzing in the ears(tinnitus).

Treatment with alpha blockers (such as Clonodine, Hytrin, etc.), as well as newer antidepressants such as Trazodone or Zoloft, provide excellent relief for the above symptoms (figure enclosed) and Muscle relaxants such as Baclofen and Trizanidine.

At times the original injury that has caused RSD may cause retinal detachment (damage to the retina of the eye) or bleeding of the eye. For this reason, the patient should have careful eye examination by an ophthalmologist as well.



H. Hooshmand, M.D.


__________________________________________________ ____________________________________

"WHAT IS RSD?"
"WHAT IS SYMPATHETIC ANYWAY?"



REFLEX SYMPATHETIC DYSTROPHY (RSD)

To define Reflex Sympathetic Dystrophy (RSD) one should understand the terminology of sympathetic and parasympathetic nervous systems. There are two different types of nervous systems controlling the body. One is the so-called "somatic" nervous system which has clear-cut anatomical structures and is controlled by the cerebral cortex (cerebral hemispheres) in a relatively volitional manner. We see, hear, touch, taste or smell something, and volitionally and knowingly respond positively or negatively towards the stimulus. We can influence our response through the judgment of higher centers of the brain (cerebral hemispheres). This is the "somatic" system which is strongly influenced and controlled by our conscious mind.

The other system is the so-called autonomic system. The name implies that it is autonomous (kind of having a mind of its own). It is almost autonomous but it can be influenced to a certain extent by conscious brain as well. This system is quite primitive and old (from evolutional standpoint). Even a worm has an autonomous nervous system. If one does an experiment by warming up one end of a fish tank water and cooling the other end of the; the worm will go from one extreme to the other and eventually will reside halfway between the two extremes of temperature in the mid portion of the fish tank. The worm does not need a brain to decide where to retire. The autonomic system does the job for it.

The autonomic nervous system concerns itself with preservation and protection of the "Internal Environment". For example, in warm blooded animals the autonomic nervous system keeps the temperature inside the body around 99º Fahrenheit (37 ºC).

To protect the internal environment, the autonomic nervous system has two main components.


1.The sympathetic system.


2.Theparasympatheticsystem.

The sympathetic system is a fight component of the "Fight and Flight" reflexes of the autonomic nervous system. On the fight end part of it the sympathetic system increases the internal temperature, raises the blood pressure, strengthens the protective function of the skin, makes the skin cold so that there would be no waste of temperature, makes the skin sweat excessively (so that there would be no extreme increase of the internal temperature); and increases muscle metabolism, bone circulation, circulation of the brain and guts. The end result is the animal is ready to fight. On the other hand, the parasympathetic system that is the balancer of the other end of the autonomic system (the flight system), drops the blood pressure, slows down the pulse, relaxes the muscles, and preserves energy by cutting down the calories burned in the body. As such, the parasympathetic system works the opposite of the sympathetic system. The two systems are totally independent and one cannot give a patient parasympathetic enhancing medications in the hope of cooling the sympathetic and vice-versa.



THEN WHAT IS RSD?


RSD is one form of disturbance of the function of the autonomic nervous system. Simply having a hyperactive sympathetic nervous system does not make RSD. The disturbance of the autonomic system comprises several diseases, some acquired, some genetic, some metabolic, some traumatic, etc.

Some examples of dysautonomias "disturbances of the autonomic nervous system" are attacks of hypotension (low blood pressure), congenital absence of sweating, and neuropathic pain syndrome.

The latter category of chronic neuropathic pain syndrome refers to the conditions that are not exactly necessarily reflex sympathetic dystrophy, but have an abnormal sympathetic component to them. They share sympathetically maintained pain (SMP) with RSD but they are not RSD.

Examples of such chronic neuropathic pain are post-hepatic neuralgia (pain accompanying and following shingles), neuropathic diabetic neuropathy, acute neuropathic pain accompanying bee stings, snake bites or spider venom stings as well as involvement of the sympathetic nerves due to the systemic AIDS infection.

The neuropathic pains are not at all synonymous with RSD. They do not even in any way resemble RSD. In some cases, however, they can end up with RSD.

The chronic neuropathic pain syndrome is far more common than the true clinical picture of RSD.



CAN RSD BE MORE CLEARLY DEFINED?



RSD is a definitive chronic pain syndrome called by several different names such as reflex sympathetic dysfunction, (stage I), reflex sympathetic dystrophy (stage II), reflex sympathetic atrophy (stage III), late stage RSD complicated by disturbance of immune system, suicidal and fetal tendency, cancer, heart attack or stroke (stage IV), complex regional pain syndrome (CRPS) which encompasses all different forms of RSD as well as the causalgic RSD, causalgia (burning, stabbing, constant pain, acting more like an epileptic seizure), shoulder-hand syndrome, sudeck's atrophy (circa 1900), traumatic vasospasm of Lehman (1934), mimocausalgia (1973), minor causalgia (1940), and half a dozen other names.


In medicine there is a trend. When a disease becomes confusing, the physicians become desperate and give it new names. Each of the above almost dozen names reflect some features of RSD.

Merskey and Bogduk in January of 1994 defined the syndrome as follows (IASP Press, Seattle classification of chronic pain 2nd edition)[1]: CRPS TYPE I is a syndrome that usually develops after an initiating noxious event, is not limited to the distribution of a single peripheral nerve, and is apparently disproportionate to the inciting event. It is associated at some point with evidence of edema, changes in skin blood-flow, abnormal sudomotor activity (sweating) in the region of the pain, or allodynia or hyperalgesia. They also clarify in the main features of CRPS (RSD). "The symptoms and signs may spread proximally or involve other extremities. Impairment of motor function is frequently seen". They clarify associated symptoms and signs and specify "atrophy of the skin, nails, and other tissues, alterations in hair growth, and loss of joint mobility may develop. Impairment of motor function can include weakness, tremor, and in rare instances, dystonia. Symptoms and signs fluctuate at times. Sympathetically maintained pain may be present and may be demonstrated with pharmacological blocking or provocation techniques. Affective symptoms of disorders occur secondary to the pain and disability. Guarding of the affected part is usually observed".

This is a long but relatively comprehensive definition of RSD. Building on the basis of this comprehensive definition of RSD, one can come to the conclusion that RSD is a syndrome with multiple manifestations which require the following minimal symptoms and signs for the condition to be called RSD (CRPS).


1. Pain: constant, burning pain, and in some forms at times during the course of the disease, stabbing type of pain (causalgic). The pain is relentless and is invariably accompanied by allodynia (even simple touch or breeze aggravating the pain) and hyperpathia (marked painful response to even a simple stimulation).

2. Spasms in the blood vessels of the skin and muscles of the extremities. The spasms in the blood vessels result in a cold extremity. The muscle spasms result in tremor, movement disorders such as dystonia, flexion spasm, weakness and clumsiness of the extremities, and tendency to fall.

3.RSD is accompanied by a certain degree of inflammation in practically all cases. This inflammation may be in the form of swelling (edema), skin rash (neurodermatitis), inflammatory changes of the skin color (mottled or purplish, bluish or reddish or pale discolorations), tendency for bleeding in the skin, skin becoming easily bruised, inflammation and swelling around the joints as well as in the joints (such as wrists, shoulders, knee, etc.) which can be identified on MRI in later stages, and secondary freezing of the joints.

4.The fourth component and pre-requisite of diagnosis of RSD is insomnia and emotional disturbance. The fact that the sympathetic sensory nerve fibers carrying the sympathetic pain and impulse up to the brain terminate in the part of the brain called "limbic system". This limbic (marginal) system which is positioned between the old brain (brainstem) and the new brain (cerebral hemispheres) is mainly located over the temporal and frontal lobes of the brain. The disturbance of function of these parts of the brain results in insomnia, agitation, depression, irritability, and disturbance of judgment. Insomnia is an integral part of an untreated RSD. So are problems of depression, irritability and agitation.

So the clinical diagnosis of RSD is based on the above four principles rather than simply excluding RSD and finding some other cause for the patient's pain.




The Four Duck Principle


Principle 1: Afferent : Allodynia, hyperpathia.
Principle 2: Efferent: Muscle spasm, cold extremities, paresis, tremors.




Principle 3: Inflammation : Edema, ulcers, skin rash, MRSA.
Principle 4: Limbic System : Dysfunction, poor memory and judgment, insomnia, depression.





Illustrations By: Mary Trent




Other laboratory and ancillary tests are helpful in confirming the diagnosis but if the results are negative they don't rule out RSD. For example, bone scan has 55 to 65% sensitivity of positive results in RSD so the other 35% of the patients still have RSD in the face of negative bone scan.


The thermography may be positive and helpful in confirming the diagnosis of RSD but at least 10% of RSD patients do not have the positive thermographic test. This is because of symmetrical involvement of RSD in both extremities. Thermography also has the handicap of tests such as MRI in that it can show false-positive results showing temperature changes in the absence of the symptoms and signs of RSD.

Phentolamine IV nerve block test is probably the most sensitive test to confirm RSD in the earlier stages (stages I and II within the first two to three years of the disease). However, as the disease becomes chronic, the longstanding constriction of the blood vessels causes disturbance of the circulation in the peripheral somatic nerves with resultant involvement of the somatic sensory nerves as well. As a result, the patient does not show a pure sympathetically mediated pain (SMP) but can show sympathetically independent pain (SIP) with no relief from Phentolamine in late stages of RSD.

In conclusion, RSD is a clinical bedside diagnosis. Not every hyperpathic pain is RSD. Not every SMP is RSD. SMP can be due to a simple post-herpetic neuralgia or diabetic neuropathy but that does not make RSD.

"Now that RSD has been diagnosed by the above criteria, what is the nature of the illness, manifestations, and treatment of RSD?"

RSD, as defined above, usually develops after a minor trauma. There are precipitating factors that enhance the development of RSD. These consist of immobilization of the extremity with cast or brace, application of ice, and inactivity due to strong addictive narcotics and tranquilizers.

The application of ice plays a major role. In experiments regarding the conductibility of the nerve impulse to the nerves, cold has shown to play a major role. If the temperature of the extremity drops from 37ºcentigrade to 10º centigrade, then the larger somatic sensory nerves stop conducting electricity through the nerve fibers. It takes the temperature to drop to 0º centigrade (freezing temperature) for the sympathetic nerves which are small thin fibers to stop conducting. The reason is the smaller the nerve fiber the less fatty sheath of myelin (insulator) surrounds the nerve. The fat in the myelin freezes more readily with the drop of temperature and stops the conduction of the nerve impulse.

What the above implies is the fact that once the extremity is cooled down with ice to 10º temperature or lower, the normal conduction of the somatic nerves (touch, vibration, and position sense) is blocked off and the extremities left with purely the sympathetic nerve fibers function (constant burning pain).

The above clearly indicates that cooling of the extremity that had minor injury will tilt the scale towards the hyperactive sympathetic burning pain function at the expense of excluding the
normal good senses of touch, vibration and position senses.

The somatic and sympathetic sense counteract each other. The somatic sensory system inhibits and stops the provocation of the exaggerated burning pain at the spinal cord level. Cooling of the extremity selectively knocks out the inhibition of the good sensory input (somatic) and causes sympathetically mediated pain (SMP) to be the sole modulation of the sensation in the RSD extremity.

It becomes obvious that not only application of ice aggravates RSD but plays a major role in the development of RSD as well.

The application of brace type cast, wheelchair and crutches also reduces the proper sensory input and results in immobilization of the extremity. The extremity that has become immobile loses its surface temperature. The body considers that extremity inactive and not needing blood on the surface so the body constricts the surface blood vessels to preserve heat and not to waste it on an immobile extremity. This second factor of immobilization aggravates the first factor of burning pain by increasing the degree of constriction of blood vessels to the skin of the extremity.

The use of addicting narcotics and benzodiazepines (tranquilizers), results in withdrawal pain every 4 to 5 hours. The use of such addicting medications puts an end to the brain manufacturing its own narcotics and BZs. As a result, 4 to 5 hours after the administration of such medications, even though the patient does not have a new injury affecting his body, feels withdrawal pain because of the lack of endorphines and endoBZs.

The combination of the above three factors, use of ice, immobilization and addicting drugs, exaggerates the SMP (sympathetically maintained pain) due to the original minor trauma.

As the condition becomes chronic, the other aspects of this syndrome complete the clinical picture. Inflammation develops, insomnia, agitation and depression affect the patient's diurnal cycle, deprive the patient of resting well and sleeping normally at night and the end result is the full-blown picture of RSD.

The original injury may involve any part of the body, but the most common areas affected by this type of sympathetic pain (i.e. constant burning pain, accompanied by severe anxiety, depression and muscle spasm) are the hand, elbow, knee, and foot.

In the United States, over five million patient suffer from this extremely painful and disabling illness called by many names, including reflex sympathetic dystrophy (RSD), sympathetic dysfunction syndrome (SDS), and causalgia, to name a few. This unusual, but severe painful condition is caused by disturbance of the function of the sympathetic nervous system (SNS).

Normally, the sense of pain is perceived through two separate channels in the body. The most common type of pain is transmitted through the nerves that end up in the cortex of the brain, over the vertex of the head (parietal lobe). This somatic pain is temporary, clear-cut and focalized. As the area of nerve damage is healed, the pain disappears.

In contrast to the somatic pain, the sympathetic pain terminates in a more primitive part of the brain, called the limbic system [2]. This is the area of the brain at the margin of brain stem and neocortex (frontal and temporal lobes). It controls emotion, memory, and judgment. The end result is insomnia, agitation, irritability, poor judgment and depression (Tables 1 and 2).



Table 1
Pain Perception

1. Somatic (simple common pain)
Parietal Cortex
2. Sympathetic (Neuropathic)

3. Bilateral Limbic System / Anterior Frontal Temporal Lobes [2]






Table 2
RSD Components

1. Sensory: Burning Pain

2. Motor: Cold Extremity Tremor/Flexor Spasm [3,4]

3. Inflammation: Swelling, Skin Rash, Bruising of Skin,

Osteoporosis, Fractures, Fluids in Joints

4. Limbic System Dysfunction

(Emotional Control Centers of Temporal and Frontal Lobes):

Insomnia, Agitation, Depression, Poor Judgment




As the condition becomes more persistent and chronic, the physician unknowingly perpetuates and aggravates the condition by the good intention of trying surgical procedures in the area affected by RSD.

The disease was first recognized by the Civil War surgeon from Atlanta (Dr. S.W. Mitchell); however, even a century later, this condition remains enigmatic, and is often diagnosed too late for successful treatment; not infrequently, it is complicated by unnecessary surgical operations, along with addicting narcotic and tranquilizer treatment. Any operation in the injured area can result in new scar formation and therefore a new source of pain. The treatment with narcotics and tranquilizers deprives the brain of it's own endogenous hormones (endorphines); this causes a new source of pain due to drug dependence. The scar of surgical procedure, added to drug dependency causes rapid deterioration; at this point, the treatment becomes the source of the disease.

Eventually, the four major manifestations of RSD evolve (see RSD Components, Table 2).The combination of a constant burning pain, which is instigated by even a simple touch (allodynia, muscle spasm and tremor, anxiety, depression and agitation, may result in a confusing, confounding and frustrating clinical picture, making the diagnosis and proper treatment quite difficult.

As a result, the source of this condition is mistaken for "psychological causes; e.g., malingering, hysteria and hypochondriasis.



In 1992, Doctor Mary E. Lynch had found no significant pre-existing psychopathology in RSD patients[5].

As the disease becomes chronic, it goes through four stages; these stages are not distinctive or clear-cut, but develop in an overlapping fashion. Stages I and II are the earliest and easiest to treat. If the disease is diagnosed and properly treated in the first six months, then stages III and IV shall be aborted. Any attempt at proper treatment, in the form of physical therapy or sympathetic block, will prevent serious complications seen in stage III and IV. (Table 3) As a result, because the classical advanced complications are not seen in partially treated patients, the clinician does not arrive at the proper diagnosis of RSD.

The staging of RSD is not as critically done on the basis of dysfunction (stage I) meaning abnormal function of the sympathetic system in the extremity, dystrophy (stage II , meaning trophic and inflammatory changes, skin changes and other signs of inflammation), atrophy (stage III, meaning usually minimal degree of atrophy in the involved muscles), or stage IV (meaning disturbance of the immune system, suicidal attempts, stroke, heart attacks, intractable hypertension and chest pain, and in some cases development of cancer). The prognosis is more related to the temporal development of the above four stages.



Table 3

Stages of RSD

Stage I: A sympathetic dysfunction with thermatomal distribution of the pain. The pain may spread in a mirror fashion to contralateral extremity or to adjacent regions on the same side of the body. In stage one, the pain is usually SMP in nature.

Stage II: The dysfunction changes to dystrophy manifested by edema, hyperhidrosis, neurovascular instability with fluctuation of livedo reticularis and cyanosis causing change of temperature and color of the skin in matter of minutes. The dystrophic changes also include bouts of hair loss, ridging, dystrophic, brittle and discolored nails, skin rash, subcutaneous bleeding, neurodermatitis, and ulcerative lesions (Fig. 5). Due to the confusing clinical manifestations, the patient may be accused of self-mutilation and even "Münchausen syndrome." All these dystrophic changes may not be present at the same time nor in the same patient. Careful history taken is important in this regard.

Stage III: Inflammation becomes more problematic and release of neuropeptides from c-fiber terminals results in multiple inflammatory and immune dysfunctions. The secondary release of substance P may damage mast cells and destroy muscle cells and fibroblasts.
Stage IV: Identifies the final stage of RSD / CRPS manifested by:

1. Failure of the immune system, reduction of helper T-cell lymphocytes and elevation of killer T-cell lymphocytes. This is in contrast to the opposite, up-regulated function of immune system in early stages.

2. The hypertension in early stages due to alpha-1 up-regulation reverses to eventual exhaustion and to the common occurrence of orthostatic hypotension in this late stage. Blood pressure changes in this stage are due to autonomic failure. The failure of the sympathetic system exaggerates the response to drugs that lower or raise the blood pressure.

3. Intractable generalized extremity and visceral edema involving the abdomen, pelvis, lungs, and extremities due to long-standing disturbance of sodium-potassium and calcium magnesium pumps usually left untreated for several years. The same organs may eventually be subject to multiple abscesses due to failure of immune function.

4. Ulcerative skin lesions.

5. High risks of cancer and suicide.

6. Multiple surgical procedures seem to be precipitating factors for development of stage IV.

This late stage is almost the flip side of earlier stages, and points to exhaustion of sympathetic and immune systems. Ganglion blocks in this stage are useless and treatment should be aimed at improving the edema and the failing immune system.




The use of addicting narcotics and benzodiazepines (tranquilizers), results in withdrawal pain every 4 to 5 hours. The use of such addicting medications puts an end to the brain manufacturing its own narcotics and BZs.

As a result, 4 to 5 hours after the administration of such medications, even though the patient does not have a new injury affecting his body, feels withdrawal pain because of the lack of endorphines and endoBZs.

The combination of the above three factors, use of ice, immobilization and addicting drugs, exaggerates the SMP (sympathetically maintained pain) due to the original minor trauma.

As the condition becomes chronic, the other aspects of this syndrome complete the clinical picture. Inflammation develops, insomnia, agitation and depression affect the patient's diurnal cycle, deprive the patient of resting well and sleeping normally at night and the end result is the full-blown picture of RSD.

The one extreme in the case of major causalgia with significant damage to the sympathetic nerve, the status 1 through 3 can develop in a matter of weeks or a few months.

On the other extreme, for example in the case of heart attack or stroke causing RSD, the stages evolve in a very slow fashion and it may take a few years before stages III and IV are seen.

The faster the stages develop, the more severe the RSD and the treatment should be applied in a more aggressive fashion.

On the other hand, even a partial or minimal treatment of chronic stages of RSD can change the clinical picture of stage III (atrophy) back to stage II or stage I. That is a good sign, but that does not mean that the patient's condition is mild just because the patient is in stage I. The more chronic the disease the more likely the persistence of the symptoms and complications even though the bed side examination shows reversal to stages I and II from stages III and IV.

If properly treated with extensive physical therapy, heat, mobilization, exercise and sympathetic nerve blocks, the success rate for full recovery in the first six months (stages I and II) is better than 80% [6].



SPREAD OF THE DISEASE



Even in the early stages, laboratory tests such as triphasic bone scanning or thermography show a spread of the disease from one side to the other. The headache and facial pain becomes bilateral, the facial pain is complicated by dizziness, tinnitus (buzzing in the ear). In the later stages of the disease, the spread is both horizontal and vertical (e.g., from right arm to left, down the legs). The reason for this spread is the anatomical structure of the sympathetic nervous system. The majority of the Sympathetic nerve fibers do not allow the standard somatic nerve fibers, but follow the wall of the blood vessels and end up in the chain of clumps of the nerve cells, called sympathetic ganglia", which are present on each side of the spine. Input of pain into any part of these chains of nerves causes the impulse to spread both vertically and horizontally[7]. This is the main reason sympathectomy or removal of the ganglia is fraught with an extremely high percentage of failure.

This complex clinical picture of the spread of this disease has played a major role in confusing and delaying the proper diagnosis and treatment of RSD. to begin with, the injury causes such a small scar that may be barely visible. This is followed by a constant burning pain, severe neck pain and headache, spread of pain to the opposite side, followed by dizziness, fatigue, insomnia, agitation and irritability.

On this background, the patient may develop pain in the arm, tremor of the hand, may have trouble walking, spasms in the legs, and may end up in a wheelchair. It is obvious that such a patient may be viewed as a neurotic, depressed, and a hypochondriac.

The condition is further compounded by the fact that the patient has normal MRI, CAT scans, and x-rays. The pain is a physiological phenomenon, due to the disturbance of small sympathetic nerve fibers; CAT scan and MRI will not show such an abnormality. An individual who suffers a heart attack and goes to the emergency room, has a normal CAT scan and MRI in the face of a potentially fatal disease. By the time MRI is abnormal, showing fluid in the involved joints or damage to the bone due to increased circulation in the deep structures, the disease is quite advanced and easy to diagnose.

Eventually, the spasm may spread to the truncal muscles; as a result, an accordion-like jamming effect of the vertebrae evolves, with resultant bulging of the lower lumbar discs noted on MRI. This may result in unnecessary surgical operation. The RSD causes constriction of blood vessels to the hands; in this clinical picture, the patient is often mis-diagnosed as carpal tunnel syndrome, tardy ulnar nerve palsy, or thoracic outlet syndrome.

Not infrequently, such patients undergo multiple operations over the arms and cervical and lumbar spine regions, with rapid acceleration and deterioration of the RSD.

The worst risk factor, and the cardinal sin, is amputation of a limb. If the patient has any sympathetic mediated pain, amputation is going to multiply the disease by several times, due to the fact that the stump of the Amputation causes scar formation at the cut ending of the nerves with marked exacerbation of RSD in the most severe form, called "Causalgia".

Even without application, surgical procedure over the inflamed area of involvement of the RSD (such as ankle, knee or wrist), is a major aggravator of RSD which overnight changes as stage I RSD to stage III or later.

The Three areas that are most commonly and unfortunately operated on are:

1.Wrist according to the diagnosis of carpal tunnel syndrome. This has already discussed in the RSD quiz related to carpal tunnel syndrome. Simply put, carpal tunnel syndrome rarely causes RSD but in rare cases of RSD the inflammation of the soft tissue at the wrist results in a clinical picture identical to carpal tunnel syndrome (CTS). This form of carpal tunnel syndrome is the effect not the cause. It is the result of RSD rather than being the cause of RSD. In this type of CTS, the entire hand, wrist and forearm are quite hypopathic, allodynic and sensitive to touch in contrast to the true somatic carpal syndrome. In this form of RSD, treatment with nerve blocks and anti-inflammatory medications Baclofen, moist heat and Epsom salt clears up the symptoms and signs of CTS. On the other hand, surgery ends up with disastrous results.

2.The same is true in the case of so-called tarsal tunnel syndrome which is over-diagnosed and over-treated universally by the podiatrists and surgery over the tarsal tunnel on the ankle rapidly deteriorates the already existing RSD.

3.The same is true with a lot of minor injuries to the knee with full-blown clinical picture of cold extremity, flexion, weakness and atrophy of the muscles around the knee, difficulty with weight bearing, severe constant burning pain, all of which prompt the surgeon to explore the knee with obvious disastrous results.

Opposite to the prevalent notion of "treat the source" the proper principle should be treat the RSD and then see what happens to the so-called source.



Even nerve blocks should not be done in the area of inflammation of RSD (over the wrist, ankle, dorsum of the foot, dorsum of the hand or the knee). Instead the nerve blocks which are very effective in treatment of RSD, should be done in axial area (over the spine) where the nerves enter and exit from the spinal cord to the involved part of the extremity.

Simply said, do not needle, amputate, or operate the area of inflammation of the RSD.



DIAGNOSIS


The diagnosis is achieved by the physician's familiarity with the triad of RSD, as mentioned above. Confirmatory tests, such as beneficial effect from sympathetic nerve block, as well as the use of bone scan or thermography are quite helpful. None of the above tests yield 100% positive diagnostic proof. Even sympathetic nerve block is positive and relieves the pain in early stages of the disease. In the later stages, there has been enough damage - due to vasoconstriction - in the involved area, that non-sympathetic pain contaminates the clinical picture and the patient does not receive 100% relief from the nerve block.


TREATMENT



Early diagnosis in the first six months to maximal two years is the key to successful treatment [6]. Surgical procedures have no place in treatment of RSD. Sympathectomy or removal of a part of the chain of sympathetic ganglia on the side of the spine) has an extremely high rate of failure. It has been reported to help the war type of RSD, which is quite different from civil type. In the war type, the soldier is a young teenager who responds favorably to treatment, regardless of the mode of treatment. The war time RSD is due to high velocity damage to the nerves in the proximal parts of the extremities and sympathectomy, even in these cases, has a high rate of failure in the long run. The civil type of RSD is due to a small damage of the sympathetic nerves in the central or peripheral nervous system.

If the patient lives longer than five years, the rate of failure from sympathectomy is over 80%. The scar of the surgical procedure becomes a new source of RSD. Removal of a part of sympathetic ganglia does not prevent spread of the disease in the areas of the body where the sympathetic nerves have been removed. This is due to the fact that the adjacent sympathetic nerves eventually compensate for the lack of sympathetic function due to surgery.



SPINAL STIMULATORS



Insertion of epidural spinal stimulators has been quite vogues. In our comparison of 41 RSD patients treated with spinal stimulators vs. 40 non-RSD chronic pain patients who received the same treatment, the RSD group of patients had only maximum three and one half to four months relief of pain. Afterwards, the stimulator acted as a foreign body and became a new source of RSD. The reason may be due to the fact that the stimulators are digital in nature with predicted rhythmic stimulation, whereas the pain of RSD is practically constant and analog (variable) in nature.

No single physician is smart and potent enough to treat RSD. Successful treatment requires a teamwork of physical medicine, anesthesiology, and neuropharmacology physicians. The keys to successful treatment are early diagnosis, early mobilization and extensive physical therapy, and early detoxification of the patient from addicting narcotics, alcohol and addicting tranquilizers.


The anesthesiologist should interrupt the sympathetic hyperactivity by doing repetitive, successive (six) nerve blocks, combined in the same day with physical therapy and exercise. Discontinuation of ice and all other assistive devices, such as wheelchair, brace, cast, walker, etc., is essential.

The addicting drugs should be replaced with the treatment of choice for chronic pain in the form of newer-generation antidepressants, Paxil, Zoloft, and Trazodone, which are not trycyclic antidepressants. Trazodone is the treatment of choice to replace the tranquilizers and sleeping pills. It provides normal sleep, as well as prevention of chronic pain. The patient can be detoxified quickly and easily by discontinuation of the narcotics and replacement with nonaddicting ones, such as Stadol. The use of muscle relaxant, Baclofen, which selectively works on the spinal cord, counteracts the spasm, clumsiness and tremor.



INFUSION PUMP



In severe brain or spinal cord injuries that result in severe crippling spasticity, the infusion pump can be very effective in the treatment of spasticity. Unfortunately, not enough infusion pumps are being used for treatment of severe head and spinal cord injuries. With the use of Baclofen in the pump, such victims of severe crippling spasticity can become mobilized and can be spared from life-threatening inactivity and bed sores.


The infusion pump has been used for treatment of severe pain. In our studies of over 400 cases of advanced RSD, over three dozen patients have been treated with infusion pump, with close to 90% success rate. Through the pump, a drip irrigation form of pain medication is introduced to the spinal fluid. The pain medication given in one month is equivalent to the amount of medication given in two to three days by mouth or by IM injection.

Infusion pump should not be mistaken with other forms of narcotic administration. The infusion pump is totally different and practically opposite to administration of narcotics in the muscle (IM), IV, by skin patch, or simply in the epidural space.

The intrathecal infusion pump (administration of the medication directly to the spinal fluid that surrounds the brain and spinal cord), provides direct access to the brain and spinal cord bypassing liver, kidney and other organs. As a result, the patient requires only 1/20 monthly dose of the narcotic to provide complete relief of pain. In addition, when the pain is optimally achieved by use of as little as 1 to 7 mg a day (usually 3mg a day) of Morphine sulfate, if the patient for other reasons has pain (such as drinking alcohol or simultaneously taking other addicting narcotics by mouth), increasing the dosage of Morphine in the spinal fluid over and above 9mg per day, causes recurrence of severe pain. This is because the system is so flooded by such a strong dose of narcotics that the brain does not form its own endorphines, and the large doses of Morphine in the pump only causes drowsiness, causes the patient respiratory trouble, but does not completely control the pain.

The above phenomenon emphasizes the importance of optimal small dose of narcotic infusion in the spinal fluid which is obviously non-addicting. When distress is violated by increasing the dosage of medicine in the pump, then it becomes like any other form of addicting narcotic administration. The patient develops severe pain due to the fact that the brain cannot form its own endorphines. If the brain manufactures its own endorphine in the face of large doses of narcotic applied in the spinal fluid, then the patient faces the risk of dying from arrest of respiration. So it becomes obvious that the infusion pump is not just another form of giving addicting medications. It works because a very small amount (usually 1/20 to 1/30 dose) of pain medication is given in the form of drip irrigation directly in the spinal fluid with complete control of pain and complete relief of symptoms and signs of RSD.



DIET



The use of proper diet, with avoidance of chocolate (phenyletholamine), hot dog, liver and sausage, and alcohol is essential in management of RSD.



REFERENCES



1. Merskey H, Bogduk N.: Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. Second Edition. Task Force on Taxonomy of the International Association for the Study of Pain. Merskey H, Bogduk N, Editors. IASP Press. Seattle, WA 1994.



2.Benarroch EE: The central autonomic network: functional organization, dysfunction, and perspective. Mayo Clin Proc 68:988-1001 1993.

3. Schwartzman RJ, Kerrigan J: The movement disorder of reflex sympathetic dystrophy. Neurology 40:57-61 1990.

4. Yokota T, Furukawa T, Tsukagoshi H: Motor paresis improved by sympathetic block a motor form of reflex sympathetic dystrophy? Arch Neurol 46: 683-687 1989.

5.Lynch ME: Psychological aspects of reflex sympathetic dystrophy : a review of the adult and pediatric literature. Pain 49:337-47 1992.

6. Poplawski ZJ, Wiley AM, Murray JF: Post traumatic dystrophy of the extremities. J Bone Joint Surg [Am] 65:642-655, 1983.

7. Appenzeller O: The Autonomic Nervous System: An introduction to basic and clinical concepts, 4th rev, Elsevier 1990.



H. Hooshmand, M.D.

Hi Roz,

and thank you for your hopes that I'm doing well; I'm beginning to suspect that some here may not share those hopes.

As I understand what you're saying, based on the abstract you include, you believe that infection is the underlying cause of some ischemic strokes and my be the cause of your RSD.

I would argue that every pro-inflammatory cytokine and every other marker of infection is found in the immune response to trauma, which is exactly the same as the immune response to infection or to pathogens.

Ischemia-reperfusion injury, is the result of a massive and uncontrolled immune response to physical trauma. This out of control response is rare, but it is known to occur.

Like RSD, IRI begins with physical trauma to tissue, followed by inflammation and then tissue hypoxia. Stage I of RSD is clearly inflammation, and stage II presents with cyanosis: proof of tissue hypoxia.

Unlike RSD, IRI is known to be treatable, if not curable, by using hyperbaric oxygen. If RSD is IRI, it too is treatable by the same thing. I don't claim that HBO can cure IRI or RSD, but I know that it has resulted in significant reduction of signs and symptoms of these "two"? disorders, and that this therapy is less expensive -- and safer -- than drugs.

I hope this answers your questions, and if it doesn't, please ask more...Vic

Vicc

" It is visible evidence of death, and nearly every incident of dark cyanosis is treated as an emergency that must be treated to save the life or limb of the patient. It is ignored in only one disease: "

Not really so,we have always been taught that someone who presents with a severely blanched limb is actually displaying more a sign of impending death of tissue and to say it is ignored in one disease, do you mean that no pain management team observe cyanosis in their patient or consider it one of the possible symptoms of RSD/CRPS? Because I refute that statement---I have had sympathetic nerve blocks because of cyanosis that have indeed improved the colour and temperature of my skin. If that is so then how do we explain the improvement is not neurological? How can you speak with so much conviction about our doctors when you really can't have any idea about those that you have never come in contact with? You can't keep criticising the medical profession en masse as you do, it is simply unfair to those who spend their lifetimes working on a way to make our lives a little better than they are.
Vicc, please realise you are continuing to become irate at those of us who are merely asking for a reason, any reason to support the fact that all the "experts" are wrong and all the artilcles available to read about RSD/CRPS state the neurological background of this disease.
Our requests of information are met only with your indignation and often fury that we are questioning you! I am ready and willing to alter my thoughts and perceptions about this disease but I must have a valid reason backed up with the science behind it to do so.
As I have repeatedly said, I am looking for a way to try and understand your view that RSD is an IRI when not all RSD/CRPS sufferers display cyanosis as a symptom.

Tayla

Amber,

I have no intention of replying in detail to doc H's arguments and claims.

He lists many complications and consequences of RSD that have not been suggested by anyone else, and many of them are clearly the result of medications and the stress of suffering from an incredibly painful and presumed to be incurable disorder.

He belief that the SNS is causally involved in RSD has been repudiated by all but a small minority of RSD "experts" (those who publish journal articles about this disease).

He offers absolutely no research in support of his fantastic claims.

I do not trust and purported neurologist foolish enough to say: The sympathetic system is a fight component of the "Fight and Flight" reflexes of the autonomic nervous system. and then asserts: On the other hand, the parasympathetic system that is the balancer of the other end of the autonomic system (the flight system), drops the blood pressure, slows down the pulse, relaxes the muscles, and preserves energy by cutting down the calories burned in the body.

"Fight or flight" involves the sympathetic nervous system preparing the subject to defend (fight) or run like Hell (flight). Flight is not a resting function, and anyone who claims that it is, doesn't know much about neurology.

I asked for research showing a causal link between traumatic nerve damage and RSD, not a bunch of opinions from someone who knows this little about neurology.

I guess its obvious that I have little use for doc H...Vic

Tayla,

You wrote: Our requests of information are met only with your indignation and often fury that we are questioning you! Not so. Anyone reading my replies has plenty of evidence that requests for information receive information. My indignation is reserved for people who deliberately, maliciously and constantly misquote me and falsely summarize my views.

I have asked that if you insist RSD is the result of a traumatic nerve injury, that you provide research supporting that view, and you only reply with accusations about me. I repeat: If you know of any research demonstrating that the signs and symptoms of this disease are caused by a nerve injury, please show it to us.

I don't claim that physicians who treat RSD are incompetent or dishonest. Physicians in clinical practice necessarily rely on information provided by experts. Thus I do claim that those who set themselves as experts by publishing articles about this disease don't seem interested in proving the claims they make.

On the other hand, I personally believe that any physician or treatment team that urges that RSD patients try taking extremely dangerous anti-psychotic drugs, in the hope that it might help their disorder, are most likely too dangerous to be allowed to practice medicine...Vic

Hi Vicc,

HBO Therapy should work if it is something viral, bacteria or fungal in origin. Now I think I had a rough reaction in HBO chamber because the fellow that operated the chamber took the pressure level way to fast. Which could of increased toxin die off way to fast , which caused a Herxheimer Reaction. This is why maybe my oxygen levels went down so low?

http://www.silver-colloids.com/Pubs/herxheimer.html

Sometimes a Herx occurs from the mycoplasma die-off. The dead organism produces toxins, which trigger the immune system. The cytokine production of the immune system will be stimulated. The elevated cytokines (such as interferon, interleukin, tumor necrosis factor, etc.), can cause many of the initial Herx symptoms. Sometimes a Herx can be from the generation of free radicals when the immune is over-activated.

http://www.mycoplasmasupport.org/Web...H_reaction.htm

I would like to give HBO Therapy ago with a facility that knows what they are doing. Much Love, Roz

Hi again Roz,

Because of the extremely poor regulation of the HBO industry in this country, I urge anyone contemplating this therapy choose a chamber that is accredited by the Undersea and Hyperbaric Medicine Society. This is your best assurance of getting therapy by professionals who know what they're doing...Vic

Vicc,

I believe there has been article upon article submitted onto this site that does explain why RSD maybe the result of traumatic nerve injury. I have no intention of reposting them again. I believe all of those who are interested in the possible causes and treatment of this disease have accessed them, read them and come to their own conclusions.
As you are asking for us to prove this common theory about RSD , I am simply asking you for the same about your theory.
You are accusing people of deliberately, maliciously and constantly misquoting you, if this is your perception then can you not see that you could be doing the exact same to others?


Your condescending comment on those medical practitoners who may prescribe "dangerous anti-psychotics" is frivilous in the extreme as they do so because they have had patients who respond well with little or no side effects. To insist that they would continue this practice if they had patients becoming unwell because of their treatments is just another indication of your disdain for any other medical opinion other than the ones subscribed to by you.

I am speaking only for myself here but I will usually happily undertake any treatment that I have thoroughly researched and established that the outcome may well and truly be worth the miniscule risk involved.
You may disagree but I can assure you I have come to no harm in my quest for an answer to this disease and I have probably tried and tested almost everything available that has been offered.
Tayla

Hi Tayla and Angel,

If I recall rightly you are both RN's. I am just a hairdresser but I have seened alot of people with severe nerve injuries. But they don't have RSD.

So what do you think is causing the spread and nerve damage? Hugs, Roz

This debate began, at least in part, because I felt I needed to reply to the implied accusation that my use of abstracts in my research made my conclusions unscientific and unreliable.

Since then it has degenerated into what it has now become: I don't intend to play this game anymore. I have offered reasons why I believe RSD is an IRI, you have argued that there is proof that it is the result of a nerve injury, but refuse to offer any evidence.

If you want to play with me, you'll have to bring some new toys: In my thread Facts you may not know about RSD, I explained how ischemia can cause allodynia. Fair's fair; its your turn to offer evidence showing how a nerve injury can cause it.

Lets put an end to accusations and return to a more reasoned approach to this topic...Vic

.... how can you explain that when my doc does surgeries, like the SCS or PNS or the pain pump that once a RSD'er is under general anesthisia that all the symptoms of RSD go away?? When i had both my surgeries for my PNS and SCS and the revision surgeries, i was put under general anesthisia adn said that my foot went to a almost normal positiion(i have a severly inverted foot) and that all my coloring goes to normal. This also happened when i had 2 week long epidurals. And the symptoms and the inverted all came right back when the general anesthisia or epidural block was stopped. My pm doc told me this bc i asked him about the workings of RSD. He said this happens in all his RSD patients and is similar to what a blcok does, but with general anesthisia your brain is totally shut down adn it also shuts down the effects of RSD and stops the pain signals.

Now doesnt that sound like nerves to me?? I can prob find a abstract if you want me to.. or?? but this is getting rediculos and youre getting upset that we are challenging your beliefs. And we are upset that you wont just say thats its what you think and leave it at that.. you are spreading this IRI theroy into the RSD world and its not even reconized to be associated with RSD. And i know that you are trying to get the word out there about IRI, but what good does it do when you are teling the people here and they go aske there docs and they have no clue.. Thier docs arnt gonna look it up and maybe if they do they find a couple articles aobut IRI but nothing conculsive.. and you i guess have the research to prove it.. so market tell ing doctors not us!! Yes we can brign it to them, but again... they are just gona think of what "they know IRI " is and dismiss it and that makes us (RSD'er) more frustrated.

Roz, I think that RSD can attack anyone and anypart of the body. And you asked me how do i explain the spread or other people with severe nerve damage that dont get RSD. Im not sure... and im not even gona tap in there bc im not a doctor! (not being mean at all... just wanted to make it clear that IM not giveing out advise) There have been researches that say people with type A personalities get this bc they have the strength or capabilities to deal with it... i think this could be possible. RSD can start with getting a stubbed toe or bee sting... and also with invasive surgeries.. Its all the luck of the draw i guess... ???

:Melting 2:
Amber

"If we knew what it was we were doing, it would not be called research, would it?"
- Albert Einstein

Thanks for the lively debate!

Perhaps when someone investigates the one thing that is common to all the body systems that rsd affects (skin,muscle, bone, blood vessels, and nerves) we will get closer to what the cause for rsd is. It may well be that that there is no "one" cause but indeed a soup mix of causes; then maybe it's one cause but in a mix of things making up the soup. Maybe trigger is the word to use. But even then, I think ok we all have cancer cells in our body so i read but not everyone gets it. One's immune system seems to keep it in check. I have a benign tumour but I wonder what set it off really, what made it grow to where if it isn't kept in check it can be lifethreatening. Maybe everyone has the potential for rsd but only some get it because of a "something" that triggers it. Maybe there's more than one trigger.

In any case, it's good to see spirited debate.

I see some "truth" in all explanations offered here, but I am not convinced by either the rsd-IRI one or the nerve one by themselves.

All the best,
carousel

Hi Roz,

In my years of nursing I had not heard of this diisease until I got it.
My first thoughts were to blame the accident, the fractures that weren't healing for the pain.:(
For some reason it is only a small group of people who do have an inciting event, remembering that RSD has come about from insect bites and paper cuts, who do develop this problem. Something triggers a pain response that simply won't shut down long after the initial injury has healed. This is why neurologists say that it is simply that the brain remembers the pain then can't rewire itself to normal again due to dysfunction of the sympathetic nervous system.
I reckon the person who can determine why one person will respond in the form of RSD and others just flick back to normal again will be the saviour of all of us with RSD/CRPS.
Cheers
Tayla:hug:

Vicc,
You say we have not shown you proof of RSD being a nerve injury but I feel that proof is never entirely possible, however when I read the research of many very learned people who have spent years developing the theory behind the cause of RSD/CRPS then I tend to find comfort from the consistancy from these people. It also makes good sense to my level of understanding.
So when you ask us for proof you must also be expected to provide proof of your theory as from all my research I only find you that has this hypothesis.

I have repeatedly said also that I am not someone who wants to dismiss a theory such as yours unless I have absolute evidence that it is rubbish and that is what I am asking you for.
If I may I would like to respectfully ask you a question or two:-

* How does someone with a paper cut develop RSD if IRI is the cause?
* Why, if cyanosis is such a part of IRI induced RSD, are there so
many people who do not have cyanosis as a feature of their RSD?
* How do you explain that cyanosis is a transient feature in some
people with RSD whose cyanotic and cold limb will become pink and
warm following a sympathetic nerve block?
I am afraid that I do not feel that skin that so amazingly changes colour in front of my eyes after 10 mls of lignocaine has been delivered to my lumber sympathetic nerve region was tissue that cyanosed because of IRI. I have seen much skin on patients which has died due to ischaemia--it does not resolve from a nerve block, it usually needs amputating.
Could the transient cyanosis of RSD just be a plain old sympathetic vasomotor response?

You say that you don't want to play this game but I don't feel it is a game, I see it as responsible questioning from people who are becoming increasingly confused by the information that is being put out there.

Tayla

New ideas about the cause, spread and therapy of Lyme Disease
Townsend Letter for Doctors and Patients, July, 2004 by James Howenstine
Lyme Disease was initially regarded as an uncommon illness caused by the spirochete Borrelia burgdorferi (Bb). The disease transmission was thought to be solely by the bite from a tick infected with this spirochete. The Bb spirochete is able to burrow into tendons, muscle cells, ligaments, and directly into organs. A classic bulls-eye rash is often visible in the early stage of the illness. Later in the illness the disease can afflict the heart, nervous system, joints and other organs. It is now realized that the disease can mimic amyotrophic lateral sclerosis, Parkinson's disease, multiple sclerosis, Bell's Palsy, reflex sympathetic dystrophy, neuritis, psychiatric illnesses such as schizophrenia, chronic fatigue, heart failure, angina, irregular heart rhythms, fibromyalgia, dermatitis, autoimmune diseases such as scleroderma and lupus, eye inflammatory reactions, sudden deafness, SIDS, ADD and hyperactivity, chronic pain and many other conditions.

http://findarticles.com/p/articles/m...52/ai_n6110580

Reading Articles like this I have no doubt that something broke the Blood Brain Barrier in my case.

Hi Everyone,

I just want to add it's not really lyme disease. It's a WORLD WIDE epidemic problem, that's been around at least hundred's of years. The Borrelia burgorferi is the strain in the States. Their is also usually co-infections with the borreilia. The Bartonella has alot of vascular issues with it.

Borrelia afzelii
Borrelia anserina
Borrelia burgdorferi
Borrelia garinii
Borrelia hermsii
Borrelia recurrentis
Borrelia valaisiana

Hi folks,
Found this interesting article :-
Reflex Sympathetic Dystrophy Syndrome: A Chiropractic Perspective

by Edgar Romero, DC, DACNB, FIAMA
Reflex sympathetic dystrophy (RSD) syndrome, or complex regional pain syndrome, as it is now called, is, as the latter name implies, a complex series of symptoms that plagues many a patient. It is most commonly associated with pain/sensory abnormalities, vasomotor dysfunction, edema/sudomotor dysfunction, and motor/trophic changes.1 Some or all of these signs may be present with a diagnosis of RSD.
Research has shown that the predisposing factor for the condition generally lies in a peripheral nerve injury or some other injury that activates nociception at a high level, and can increase sensitization in the central nervous system.2 The pain can be in one limb or can progress to encompass the entire body. There is no psychological component to RSD, but many patients are severely depressed because of the constant pain, lack of sleep, and total disruption of lifestyle that occurs with the condition.2 It has been determined through further studies into this devastating condition that the etiology is in fact central, subsequent to the peripheral lesions that initiate the syndrome.3
According to the current medical model, physical therapy is the cornerstone of first-line treatment, with moderate cases requiring adjunctive analgesics, such as anticonvulsants and/or antidepressants. Use of opiods is not uncommon for those in too much pain to participate in physical therapy. For severe cases, anesthetic blockade, sympathetic/somatic blockades, spinal cord stimulation and spinal analgesia are all part of the treatments provided.4
A possible etiology of this pathology from a neurological point of view will be explained in this paper, with the proper treatment, including chiropractic, based on signs and symptoms. As stated previously, RSD is in many cases precipitated by some trauma or peripheral nerve injury that progresses over time to the syndrome, with associated pain and dysfunction. It must be assumed that the increased frequency of firing of the pain pathways has the effect of starting the imbalance that leads to RSD.
Nociceptive pathways have collaterals into the intermediolateral cell column (IML) of the spinal cord, which also happens to be the primary neuron of the sympathetic system. As a vasomotor component is one of the chief diagnostic indicators of the condition, one must assume that this pain barrage may be part of the initial syndrome. If this were the only factor, however, anyone who had ever been injured and felt pain would have at least some diagnostic indicators of RSD.
Although we all do experience a localized inflammatory response secondary to central vasoconstriction and peripheral dilation associated with increased sympathetic response after an injury, it is of course not to a degree that RSD would develop. Nociception does not in fact end at the spinal cord, obviously. It has rostral synapses, some of which proceed through the thalamus to the parietal cortex and consciousness. The greater numbers by far, however (76 percent, by some estimates), have collaterals that synapse in the reticular formation of the mesencephalon and the pons. The mesencephalic (or rostral) reticular formation has an excitatory effect on the cortex to increase perception. Thus, not only will a patient have difficulty sleeping secondary to an increased firing cortex, but the very perception of pain itself will also seem greater to the patient, even in the absence of continued nociception.
More importantly, the rostral reticular formation has an inhibitory effect on the medullary, or caudal, reticular formation. The caudal reticular formation itself inhibits the IML, which, to reiterate, is the primary neuron of the sympathetic system. Inhibition of an inhibitory center allows excitation to occur. Thus, the IML would be at a greater central integrative state than would normally be expected in the individual. This now gives us a possible double firing into the IML; when activated, the IML will produce a central vasoconstriction so powerful that there is likely an anoxic condition of the affected tissue.
Anoxic conditions in any tissue produce lactic acid and other nociceptive chemicals, further driving the nociceptive system and increasing the likelihood of IML firing. It can quickly become a catch-22 scenario, whereby nociception produces vasoconstriction, and vasoconstriction produces nociception. As described earlier, peripheral nerve injuries have a great likelihood of leading to RSD. With any peripheral nerve injury, it is large-diameter .


This is one article that I think gives a good explanation of how our vasoconstrictive and trophic tissue changes can be explained to be a part of a neurological disorder.
Cheers all
Tayla:hug:

Dear Tayla,

In your opinion can a infection cause, pain/sensory abnormalities, vasomotor dysfunction, edema/sudomotor dysfunction, and motor/trophic changes?

It will be to late when we are in ICU, Much Love, Roz

Does anyone else think this is a PATHOLOGY problem? Roz

Hi,

I hope everyone just gets bettter or shows some improvement at all. Much Love, Roz

Hi Roz,

I imagine that infection is just like any other assault to our body that could lead to all of the changes you mention.
I must have a look around and see if there are articles written about this.
I have major infections as a result of trophic changes--it may be another of the 'chicken and egg" problems.

ICU and I have become friends over the last few years-:mad:--bloody stupid disease.
Take care Roz---talk soon
Love Tayla:hug:

Hello everyone I hope you are all doing fine. I have a true abstract from American Journal of Pain Management from Dr. Hooshmand.

Venipuncture Complex Regional Pain Syndrome Type II
by Hooshang Hooshmand, MD, Masood Hashmi, MD, and Eric M. Phillips

Keywords: causalgia, CRPS Type I and II, neuroinflammation, sympathectomy, venipuncture
Volume: AJPM Vol. 11 No. 4 October 2001 pgs 112-124Abstract:
Venipuncture Complex Regional Pain Syndrome Type II (VP-CRPS II) is a rare and unpredictable complication of venipuncture. It is the manifestation of a minor injury leading to a severe form of CRPS. It should not be mistaken for benign forms of hematoma or phlebitis without CRPS. There is no definite causal relation with the type of needle used, nor with number of attempts at IV insertion. It is usually a rare complication of the needle accidentally injuring the microscopic microvascular C-thermoreceptor sensory nerve. Lack of experience and severity of the trauma are not proven risk factors, and there are no known preventive measures. Accidental infiltration of chemical irritants can instigate the VP-CRPS, unless the injection is discontinued immediately. Early diagnosis and proper treatment provide significant pain relief. Multimodal treatment is essential. Surgical procedures, especially sympathectomy, may exacerbate the condition and lead to irreversible therapeutic failure.

and a link with a great artical(ABSTRACT) thank you, I feel we all help by sharing our info, by sharing we gain knowledge wich in turn helps us all. Vicc dear friend please do not leave this very important discussion no one is slamming you, we all want to know how you came up with your abstract? and to say all the docs who study this are wrong is not right, is the other issue I hope you return to the discussion it helps us all when we share.
Have a pain free day you all.oh the link here it is
http://www.ajpmonline.com/search/def...294.5805671296